Influence of a high-glucose diet on the sensitivity of Caenorhabditis elegans towards Escherichia coli and Staphylococcus aureus strains

被引:7
|
作者
Lavigne, Jean-Philippe [1 ,2 ,3 ]
Audibert, Sylvain [1 ,2 ]
Molinari, Nicolas [4 ]
O'Callaghan, David [1 ,2 ]
Keriel, Anne [1 ,2 ]
机构
[1] INSERM, U1047, UFR Med, F-30908 Nimes 02, France
[2] Univ Montpellier I, UFR Med, F-30908 Nimes 2, France
[3] CHU Caremeau, Bacteriol Lab, F-30029 Nimes 09, France
[4] CHU Caremeau, F-30029 Nimes 09, France
关键词
Caenorhabditis elegans; Diabetes mellitus; DAF-16; Escherichia coli; Staphylococcus aureus; Virulence; CHANNEL AQUAPORIN-7 GENE; LIFE-SPAN; HEAT-SHOCK; DAF-16; ADIPOSE; OBESITY; MODEL; INFECTIONS; PREVALENCE; ACTIVATION;
D O I
10.1016/j.micinf.2013.04.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
It was recently observed that a glucose-enriched diet activates the insulin-like pathway in Caenorhabditis elegans, resulting in an inhibition of the FOXO transcription factor DAF-16. Because this signalling pathway is highly conserved from invertebrates to mammals and DAF-16 is a key player in innate immunity, we wondered whether a high-glucose diet, resembling the hyperglycaemic conditions in diabetic patients, would affect the susceptibility of C. elegans to bacterial pathogens isolated from different clinical situations (urinary tract or diabetic foot infections). We confirmed previous reports showing that such a diet decreases the lifespan of C. elegans fed with an avirulent Escherichia colt strain. However, glucose-fed nematodes appeared to be more resistant to most clinical isolates tested, showing that this invertebrate model does not mimic infections encountered in human diabetes, where patients show increased susceptibility to bacterial infections. This study also suggests that modulation of innate immunity in C. elegans, upon activation of the IGF1/insulin-like pathway by glucose, is not exclusively mediated by DAF-16, but also involves an additional factor that requires DAF-16 activity. (C) 2013 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:540 / 549
页数:10
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